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Age-associated Declines in Mitochondrial Biogenesis and Protein Quality Control Factors Are Minimized by Exercise Training

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Specialty Physiology
Date 2012 May 11
PMID 22573103
Citations 68
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Abstract

A decline in mitochondrial biogenesis and mitochondrial protein quality control in skeletal muscle is a common finding in aging, but exercise training has been suggested as a possible cure. In this report, we tested the hypothesis that moderate-intensity exercise training could prevent the age-associated deterioration in mitochondrial biogenesis in the gastrocnemius muscle of Wistar rats. Exercise training, consisting of treadmill running at 60% of the initial Vo(2max), reversed or attenuated significant age-associated (detrimental) declines in mitochondrial mass (succinate dehydrogenase, citrate synthase, cytochrome-c oxidase-4, mtDNA), SIRT1 activity, AMPK, pAMPK, and peroxisome proliferator-activated receptor gamma coactivator 1-α, UCP3, and the Lon protease. Exercise training also decreased the gap between young and old animals in other measured parameters, including nuclear respiratory factor 1, mitochondrial transcription factor A, fission-1, mitofusin-1, and polynucleotide phosphorylase levels. We conclude that exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis.

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References
1.
Chen H, Rainey R, Balatoni C, Dawson D, Troke J, Wasiak S . Mammalian polynucleotide phosphorylase is an intermembrane space RNase that maintains mitochondrial homeostasis. Mol Cell Biol. 2006; 26(22):8475-87. PMC: 1636764. DOI: 10.1128/MCB.01002-06. View

2.
Gomez-Cabrera M, Domenech E, Vina J . Moderate exercise is an antioxidant: upregulation of antioxidant genes by training. Free Radic Biol Med. 2008; 44(2):126-31. DOI: 10.1016/j.freeradbiomed.2007.02.001. View

3.
Radak Z, Young Chung H, Naito H, Takahashi R, Jung K, Kim H . Age-associated increase in oxidative stress and nuclear factor kappaB activation are attenuated in rat liver by regular exercise. FASEB J. 2004; 18(6):749-50. DOI: 10.1096/fj.03-0509fje. View

4.
Bota D, Davies K . Lon protease preferentially degrades oxidized mitochondrial aconitase by an ATP-stimulated mechanism. Nat Cell Biol. 2002; 4(9):674-80. DOI: 10.1038/ncb836. View

5.
Radak Z, Naito H, Kaneko T, Tahara S, Nakamoto H, Takahashi R . Exercise training decreases DNA damage and increases DNA repair and resistance against oxidative stress of proteins in aged rat skeletal muscle. Pflugers Arch. 2002; 445(2):273-8. DOI: 10.1007/s00424-002-0918-6. View